ライフサイエンスコーパス: MAO-B

1 MAO B activity was found to be widely distributed throug

2 MAO B and MAO A are more selective for the R-enantiomer

3 MAO B inhibition is therefore associated with enhanced a

4 MAO B is involved in the breakdown of dopamine, a neurot

5 MAO B messenger RNA also correlated with viral loads in

6 MAO B messenger RNA was highest in macaques with the mos

7 MAO B specific activity is dependent upon the size of th

8 MAO-B-specific monoclonal antibody (MAO B-1C2) conjugate

9 AO-B inhibitor (K(i)(A(2A)) = 260 nM; IC(50)(MAO-B) = 200 nM; IC(50)(MAO-A) = 10 muM) and dose depend

10 We previously showed that the -246/-99 MAO B promoter region exhibited the highest activity and

11 uced MAO A/B double knock-out (KO) mice in a MAO B KO mouse colony.

12 thesized compounds were evaluated for MAO-A, MAO-B, and AChE inhibitory activities as potential drug

13 nd by a decrease in the expression of MAO-A, MAO-B, and tryptophan hydroxylase in the dorsal raphe nu

14 rgyline and deprenyl even if the ratio MAO A/MAO B was approximately 1 to 10.

15 n the basis of docking studies using a MAO-A/MAO-B homology model.

16 d on the basis of docking studies to a MAO-A/MAO-B homology model.

17 targets, the first potent, dual-acting A2AAR/MAO-B inhibitors with a nonxanthine structure were devel

18 may be useful tools for validating the A2AAR/MAO-B dual target approach in PD.

19 atives previously characterized as dual AChE-MAO B inhibitors to probe the effects on both inhibitory

20 related family member Sp4 can trans-activate MAO B promoter activity through the proximal cluster of

21 RA activates MAO B promoter in both concentration- and time-dependent

22 In contrast, the properties affecting MAO B affinity were the polarity and bulk of the para-su

23 d with the membrane-bound forms of MAO A and MAO B (MAO A Y444 mutant enzymes are found to be unstabl

24 ng the monoamine metabolic enzymes MAO A and MAO B (MAO AB-deficient mice) exhibit diminished prolife

25 of the studied compounds with both MAO A and MAO B are interpreted in light of crystallographic data

26 Thus, both MAO A and MAO B contribute to the metabolism of dopamine when high

27 Human MAO A and MAO B each contain 9 cysteine residues (7 in conserved s

28 The selectivities of MAO A and MAO B for flavin analogue incorporation are found to be

29 en able to selectively detect both MAO A and MAO B from cow brain tissue with protein content as low

30 lar impact of analogous mutants in MAO A and MAO B suggests that these amino acids have the same func

31 human monoamine oxidases A and B (MAO A and MAO B) show aromatic amino acid residues oriented approx

32 oamines, because of the absence of MAO A and MAO B, cause functional alterations that are accompanied

33 tes that, though catalyzed by both MAO A and MAO B, dopamine deamination following treatment with L-D

34 tor present in the mammalian forms MAO A and MAO B, has allowed for the isolation and further structu

35 f the structures and mechanisms of MAO A and MAO B, which are pharmacological targets for specific in

36 n the mitochondrial membrane-bound MAO A and MAO B.

37 It occurs in 2 subtypes, MAO A and MAO B.

38 MAO B-I236T and mutant pair MAO A-D328G and MAO B-G319D reduced catalytic activity but did not alter

39 energy of interaction between inhibitor and MAO B residues during inhibitor egress is an effective i

40 tor of both human AChE (IC(50) = 550 nM) and MAO B (IC(50) = 8.2 nM, B/A selectivity > 1200).

41 Mutant pair MAO A-T245I and MAO B-I236T and mutant pair MAO A-D328G and MAO B-G319D

42 CSE significantly reduced MAO-A and MAO-B activities in vitro, whereas nicotine did not.

43 ght on how selective inhibition of MAO-A and MAO-B can be achieved by geometric isomers of cis- and t

44 increased research into selective MAO-A and MAO-B inhibitors.

45 nally related monoamine oxidase (MAO) -A and MAO-B is >10 microM.

46 The selective inhibition of the MAO-A and MAO-B isoforms was confirmed ex vivo in mouse brain homo

47 docking experiments carried out on MAO-A and MAO-B structures proved new information about the enzyme

48 Monoamine oxidases A and B (MAO-A and MAO-B) are enzymes of the outer mitochondrial membrane t

49 O over monoamine oxidases A and B (MAO-A and MAO-B).

50 xpression of monoamine oxidase-A (MAO-A) and MAO-B in the lateral OFC and by a decrease in the expres

51 CAs (K(I)s in the range of 0.1-90.0 nM) and MAO-B (IC(50) in the range of 6.7-32.6 nM).

52 -B, when the structures of MAO-N proline and MAO-B-isatin were overlaid.

53 which acts as a dual human A(2a) antagonist/MAO-B inhibitor (K(i)(A(2A)) = 260 nM; IC(50)(MAO-B) = 2

54 mpound is the best balanced A(2A) antagonist/MAO-B inhibitor reported to date, and it could be consid

55 MAO-B-specific monoclonal antibody (MAO B-1C2) conjugated to colloidal gold was used as a pr

56 ns 2-12 showed good inhibitory activities at MAO-B, AChE, and BChE but low selectivity.

57 Average MAO-B levels in smokers in the present study were simila

58 l cortex monoamine oxidases A (MAO A) and B (MAO B) determined.

59 Monoamine oxidase B (MAO B) catalyzes the oxidative deamination of biogenic a

60 fluorometric assay for monoamine oxidase B (MAO B) has been developed.

61 otopic membrane protein monoamine oxidase B (MAO B) is an important drug target for Parkinson's disea

62 Monoamine oxidase B (MAO B) is an integral protein of the outer mitochondrial

63 ors selective for human monoamine oxidase B (MAO B) that do not inhibit MAO A have been described in

64 osition of bovine liver monoamine oxidase B (MAO B) was investigated using size-exclusion chromatogra

65 olinesterase (AChE) and monoamine oxidase B (MAO B), a series of multitarget ligands was properly des

66 ersible inactivators of monoamine oxidase B (MAO B).

67 ecrease in the level of monoamine oxidase B (MAO B; EC 1.4.3.4) relative to non-smokers or former smo

68 bitors of monoamine oxidase A (MAO-A) and B (MAO-B) holds a therapeutic relevance in the treatment of

69 s some structural features with human MAO B (MAO-B).

70 was further studied in monoamine oxidase B (MAO-B) and cyclooxygenase-1 (COX-1) enzyme through molec

71 two monotopic proteins, monoamine oxidase B (MAO-B) and cyclooxygenase-2 (COX-2), interact with a pho

72 ated increases in brain monoamine oxidase B (MAO-B) and its ability to produce reactive oxygen specie

73 reversible inhibitor of monoamine oxidase B (MAO-B) at the conventional dose (10 mg/day oral) that is

74 AARs) and inhibition of monoamine oxidase B (MAO-B) in the brain are considered attractive strategies

75 GM1 ganglioside and the monoamine oxidase B (MAO-B) inhibitor L-deprenyl, alone and in combination, o

76 nson's disease in which monoamine oxidase B (MAO-B) is overexpressed and which emulates several featu

77 mokers have lower brain monoamine oxidase B (MAO-B) levels than comparison nonsmoking subjects and to

78 The monoamine oxidase B (MAO-B) substrate properties and distance measurements al

79 Monoamine oxidase B (MAO-B) was recently identified as a member of the family

80 ne was found to inhibit monoamine oxidase B (MAO-B) with an IC(50) of 18 +/- 7.1 muM in preliminary a

81 lavin-containing enzyme monoamine oxidase B (MAO-B).

82 eversible inhibitors of monoamine oxidase B (MAO-B).

83 linesterase (AChE), and monoamine oxidase B (MAO-B).

84 11)C]SL25.1188, targets monoamine oxidase-B (MAO-B) enzyme, found primarily in astrocytes, which meta

85 Monoamine oxidase-B (MAO-B) is a key enzyme in the catabolism of biogenic ami

86 MPTP is converted by monoamine oxidase-B (MAO-B) to its neurotoxic metabolite 1-methyl-4-phenyl-py

87 mine agonists, and monoamine oxidase type B (MAO-B) inhibitors.

88 of labeled deprenyl to peripheral MAO B; (b) MAO B can be visualized and quantified in the heart, lun

89 Because MAO B breaks down catecholamines and other physiological

90 inoic acid (RA) significantly activates both MAO B promoter activity and mRNA expression in a human n

91 azole (7-NI), a reversible inhibitor of both MAO-B and neuronal nitric oxide synthase (nNOS) activity

92 d in all known MAO B sequences except bovine MAO B, which has Phe in this position (the sequence of s

93 Brain MAO-B levels did not differ between baseline levels and

94 Brain MAO-B levels were measured by means of positron emission

95 Here we compared MAO B in peripheral organs in nonsmokers and smokers by

96 In contrast, MAO B knock-out mice do not exhibit aggression and only

97 sitions 511, 504, and 498 slightly decreased MAO B catalytic activity and had no significant changes

98 ine), and became more sensitive to deprenyl (MAO B-specific inhibitor) than to clorgyline (MAO A-spec

99 nhibition of A(2A) receptor knockout-derived MAO-B by CSC.

100 Here, we present a novel class of dual MAO-B inhibitors and NRF2 inducers with neuroprotective

101 with valuable tools for designing effective MAO B inhibitors as well as outline a method that can be

102 e the MAO B promoter and increase endogenous MAO B transcripts via the Sp1/Egr-1/Sp1 overlapping bind

103 6-tetrahydropyridine species is an excellent MAO-B substrate, behavior which may not be consistent wi

104 in a higher level of catalytic activity for MAO B than for MAO A.

105 values only 16-fold and 2.4-fold higher for MAO B and MAO A, respectively.

106 Rasagiline has the highest specificity for MAO B, as demonstrated by a 100-fold higher inhibition p

107 d was found to be an excellent substrate for MAO B (Km = 218 microM, Kcat = 435 min-1).

108 All three compounds were also substrates for MAO B with partition ratios ranging from 152 to 536.

109 stem to study the gene regulation unique for MAO B.

110 % inhibitory concentration of compound 6 for MAO-B was 227 +/- 36.8 nM.

111 line at high doses loses its selectivity for MAO-B, there is no direct evidence that it also inhibits

112 inhibitory activity (IC50 = 30 nM) and good MAO B/A selectivity (selectivity index, SI = 94) along w

113 c substituents producing compounds with high MAO B affinity.

114 isplayed good inhibitory activities and high MAO-B selectivity.

115 Human MAO B core promoter (-246 to -99 region) consists of CAC

116 2-myristate 13-acetate (PMA) increases human MAO B, but not MAO A, gene expression.

117 ignments and the crystal structures of human MAO B in complex with 1,4-diphenyl-2-butene or with tran

118 In the case of human MAO B, two tyrosyl residues (Y398 and Y435) are found in

119 hich is covalently bound to Cys-397 of human MAO B.

120 The human MAO B I199F mutant protein of MAO B binds to isatin (K(i

121 d shares some structural features with human MAO B (MAO-B).

122 dole-5-carboxamide (53, PSB-1410, IC50 human MAO-B 0.227 nM, >5700-fold selective versus MAO-A).

123 ole-5-carboxamide (38a, PSB-1491, IC50 human MAO-B 0.386 nM, >25000-fold selective versus MAO-A) and

124 t and selective MAO-B inhibitors (IC50 human MAO-B 0.612 nM, >16000-fold selective versus MAO-A).

125 zole-5-carboxamide (30, PSB-1434, IC50 human MAO-B 1.59 nM, selectivity versus MAO-A>6000-fold), high

126 amide (17, Ki human A2A, 39.5 nM; IC50 human MAO-B, 34.9 nM; selective versus other AR subtypes and M

127 class of potent MAO-B inhibitors (IC50 human MAO-B: 1.63 nM).

128 sis for the irreversible inhibition of human MAO-B by mofegiline.

129 localized to residues K149 to M222 of human MAO-B.

130 Recombinant human MAO-B and MAO-A enzyme preparations were used to determi

131 dence shows a relationship between the human MAO-B (hMAO-B) enzyme and neuropsychiatric/degenerative

132 bility to counteract ATP reduction, and (ii) MAO-B rather than NOS inhibition is the mechanism by whi

133 as to investigate the feasibility of imaging MAO B in peripheral organs in humans with PET.

134 Importantly, MAO-B elevation was found to abolish the spare KGDH thre

135 Asp-132 in MAO A (Asp-123 in MAO B) located at the entrance of the U-shaped substrate

136 ndicate that Ile-335 in MAO A and Tyr-326 in MAO B play a critical role in determining substrate and

137 n MAO A and Lys-296, Trp-388, and Tyr-398 in MAO B may be involved in the non-covalent binding to FAD

138 and Tyr-444 in MAO A (Tyr-398 and Tyr-435 in MAO B) may form an aromatic sandwich that stabilizes the

139 We tested the roles of Arg-42 and Thr-45 in MAO B by constructing mutant MAO B cDNAs which encode am

140 MAO A and their corresponding amino acids in MAO B, Lys-296, Trp-388, Tyr-398, and Tyr-435, play impo

141 26 and Asp227 are involved in FAD binding in MAO B, site-specific mutants that encode substitutions a

142 ion was increased by PMA but not involved in MAO B gene transcription.

143 ed two noncovalent flavin-binding regions in MAO B (residues 6-34 and 39-46).

144 ith lysine or Thr-45 with serine resulted in MAO B variants that retain both partial activity and par

145 have found an additional FAD-binding site in MAO B (residues 222-227), which is highly conserved acro

146 40 promoter factor 1 (Sp1) binding sites in MAO B promoter.

147 al significance of this structure, Tyr435 in MAO B was mutated with the amino acids Phe, His, Leu, or

148 hat H2O2 production via subtle elevations in MAO-B levels can result in oxidative effects on KGDH tha

149 endogenous alpha-synuclein via elevations in MAO-B levels could be abrogated by the addition of depre

150 -inactivated MAO A and pargyline-inactivated MAO B, respectively.

151 -beta-inducible early gene (TIEG)2 increased MAO B gene expression at promoter, mRNA, protein, and ca

152 In our cells, increased MAO-B activity was found to result in increased H2O2 pro

153 utation of the third RARE reduced RA-induced MAO B promoter activation by 50%, suggesting this elemen

154 nalogues of 17f, namely 18b and 19a, inhibit MAO-B with IC(50) of 68 and 48 nM, respectively, being 5

155 t, and therapeutic use of drugs that inhibit MAO-B are major challenges for future therapy.

156 spectral properties of mofegiline inhibited MAO-B show features (lambda(max) approximately 450 nm) u

157 A high dose of L-deprenyl, inhibiting MAO-B activity, (10 mg/kg, i.p. every other day for 3 we

158 levodopa (IPX066), safinamide which inhibits MAO-B, dopamine uptake and glutamate and pardoprunox whi

159 This study provides new insights into MAO B gene expression and illustrates the complexity of

160 petitive inhibitor isatin binds to all known MAO B and MAO A with similar affinities.

161 Ile-199 is conserved in all known MAO B sequences except bovine MAO B, which has Phe in th

162 -fluorodeprenyl-D2 was consistent with known MAO-B expression in the human brain.

163 Mice lacking MAO B are resistant to the Parkinsongenic neurotoxin, 1-

164 Mutant MAO A-I335Y became like MAO B, which exhibits a higher preference for beta-pheny

165 gest that detergent-solubilized bovine liver MAO B exists as cooperative oligomeric enzyme complexes.

166 activity studies published with bovine liver MAO B.

167 tion of the liver, which cannot be measured, MAO B activity is highest in the kidneys and heart; and

168 ct on the rate of inactivation of 0.1 microM MAO-B by 500 microM inactivator.

169 ifically inhibited mouse brain mitochondrial MAO-B activity in vitro with a K(i) value of 100 nm, whe

170 he X-ray crystal structure of the mofegiline-MAO-B adduct shows a covalent bond between the flavin co

171 circular dichroism spectra of the mofegiline-MAO-B adduct shows a negative peak at 340 nm with an int

172 t competitively human, horse, rat, and mouse MAO B with K(i) values in the low micromolar range but a

173 2 and Thr-45 in MAO B by constructing mutant MAO B cDNAs which encode amino acid substitutions at the

174 The reciprocal mutant MAO B-Y326I exhibited an increased preference for 5-hydr

175 both synthetic oligonucleotides and natural MAO B core promoter.

176 with Sp1 in the Sp1-binding sites of natural MAO B promoter.

177 r occupancy by Sp1 were shown at the natural MAO B core promoter.

178 rate-binding site has no effect on MAO A nor MAO B catalytic activity.

179 ated between the affinity for MAO A, but not MAO B, and the levels of 3,4-dihydroxyphenylacetic acid

180 o the left, (2) inhibition of MAO-A, but not MAO-B, increases low-dose nicotine self-administration,

181 Previously, Glu-34 and Tyr-44 of MAO B have been identified as residues which engage in n

182 xyl-terminal amino acid residues 417--520 of MAO B are not directly involved in the active site but a

183 re required for the subsequent activation of MAO B by covalent coupling of FAD.

184 mechanisms for glucocorticoid activation of MAO B gene and provides new insights into the hormonal r

185 Sp3 inhibits Sp1 and Egr-1 activation of MAO B gene expression.

186 d Sp1-activated glucocorticoid activation of MAO B promoter.

187 ssentially required for the RA activation of MAO B through two clusters of Sp1-binding sites in the M

188 bitor blocks the PMA-dependent activation of MAO B.

189 lent flavinylation and catalytic activity of MAO B, but also with noncovalent binding of FAD.

190 lent flavinylation and catalytic activity of MAO B, but not for noncovalent binding of FAD.

191 The activity of MAO B, therefore, can be determined efficiently and rapi

192 that is distinct from the FAD-PCPA adduct of MAO B.

193 (deuterium isotope effect) characteristic of MAO B.

194 ght of crystallographic data of complexes of MAO B with rasagiline and its analogues.

195 le enzyme, our assay allows the detection of MAO B activity as low as 1.2 x 10(-5) U/ml.

196 des a molecular basis for the development of MAO B-specific reversible inhibitors without interferenc

197 Distribution of the oligomeric forms of MAO B was found to be dependent upon protein concentrati

198 ood substrate for all WT and mutant forms of MAO B.

199 expression of Sp3 inhibited the induction of MAO B gene by Sp1, and the expression of Sp3 was decreas

200 ion mutants indicate that the interaction of MAO B with mitochondrial membrane is not simply anchorin

201 quantitation in organs having high levels of MAO B is improved by the use of 11C-L-deprenyl-D2, simil

202 45 with alanine resulted in complete loss of MAO B activity and FAD incorporation.

203 new insight into the molecular mechanisms of MAO B regulation by hormones.

204 In vitro methylation of MAO B promoter with 5-aza-2'-deoxycytidine, a DNA methyl

205 The human MAO B I199F mutant protein of MAO B binds to isatin (K(i) = 3 microM) but not to the t

206 We propose that reduction of MAO B activity may synergize with nicotine to produce th

207 enzyme may play a role in the regulation of MAO B.

208 Among hormonal regulations of MAO B, we have recently found that retinoic acid (RA) si

209 fied two novel transcriptional repressors of MAO B, E2F-associated phosphoprotein (EAPP) and R1 (RAM2

210 Atomistic molecular dynamics simulations of MAO B either embedded in a lipid bilayer or free in solu

211 Additional MD simulations of MAO B in complex with seven different reversible inhibit

212 ivators at proximal Sp1 overlapping sites of MAO B.

213 were correlated with increased solubility of MAO B mutants.

214 environment is required for the stability of MAO B.

215 semiquinone radical in the resting state of MAO B.

216 The x-ray structure of MAO B shows that Cys5 is located on the surface of the m

217 In contrast, an earlier study of MAO B only found evidence for an anionic flavin radical.

218 A structure is "more flexible" than that of MAO B and that clorgyline and pargyline inactivation of

219 the substrate specificity resemble those of MAO B, while others are similar to MAO A, including biph

220 e the impetus for increased transcription of MAO B and that MAO, and more broadly, oxidative stress,

221 examers appear to be composed of a trimer of MAO B homodimers.

222 indicate that CSC possesses dual actions of MAO-B inhibition and A(2A) receptor antagonism, a unique

223 The amount of MAO-B binding positively correlated with the age of subj

224 A decreased amount of MAO-B in smokers further validates the pharmacological e

225 Examination of the regional distribution of MAO-B revealed lower [(3)H]lazabemide binding to MAO-B i

226 The A(2A) receptor independence of MAO-B inhibition by CSC was further supported by the sim

227 dose of l-deprenyl yielded 70% inhibition of MAO-B in all regions.

228 Irreversible inhibition of MAO-B occurs with a 1:1 molar stoichiometry with no obse

229 well with isatin, a reversible inhibitor of MAO-B, when the structures of MAO-N proline and MAO-B-is

230 2 cell lines with subtly increased levels of MAO-B mimicking those observed during normal aging.

231 lished molecular model of the active site of MAO-B.

232 However, suppression of MAO-B does not induce developmental alterations.

233 uitable PET radioligand for visualization of MAO-B activity in the human brain.

234 2 was an activator, but Sp3 had no effect on MAO B gene expression.

235 riables, including tobacco smoke exposure on MAO B activity in peripheral organs in humans.

236 time showing the stimulating effect of RA on MAO B and new insight into the molecular mechanisms of M

237 fication of an imidazoline binding domain on MAO-B provides a new opportunity for the potential pharm

238 o localize the imidazoline binding domain on MAO-B, we labeled the domain with the imidazoline photoa

239 and protein expression, while its effects on MAO-B were minimal.

240 H(2)O(2) is produced during either MAO A or MAO B inactivation, which demonstrates that covalent add

241 mg/kg) which selectively inhibited MAO A or MAO B, respectively, striatal dopamine was increased whi

242 y and solubility of human monoamine oxidase (MAO B), 10 sequential mutants were made with stop codons

243 dase (pkDAO) or rat liver monoamine oxidase (MAO-B).

244 pecificity of labeled deprenyl to peripheral MAO B; (b) MAO B can be visualized and quantified in the

245 The most potent MAO-B inhibitors were N-(3'-chlorophenyl)-4-oxo-4H-chrom

246 , were identified as a novel class of potent MAO-B inhibitors (IC50 human MAO-B: 1.63 nM).

247 nding 6'-benzyloxy derivatives showed potent MAO-B inhibition and inverted selectivity profile.

248 Expression of the green fluorescent protein-MAO B C481 fusion protein revealed that this mutant was

249 g 5-7-fold more potent than the prototypical MAO-B inhibitor deprenyl (IC(50) = 334 nM).

250 density gradient centrifugation of purified MAO B exhibited a direct correlation between enzyme acti

251 Transmission electron microscopy of purified MAO B was performed using protein prepared by octyl gluc

252 rs with respect to their ability to quantify MAO B.

253 ound that smokers have significantly reduced MAO B in peripheral organs, particularly in the heart, l

254 nd R1 (RAM2/CDCA7L/JPO2), that down-regulate MAO B via MAO B core promoter, which contains Sp1 sites.

255 NA methyltransferase inhibitor, up-regulated MAO B gene expression in both HeLa and Caco-2 cells.

256 irreversibility than did previously reported MAO-B radioligands.

257 ments for development of specific reversible MAO B inhibitors is in a fairly mature status.

258 umulation and showed competitive, reversible MAO-B inhibition.

259 as found to be the most potent and selective MAO-B (high selectivity over MAO-A) and AChE inhibitor i

260 r novel class of highly potent and selective MAO-B inhibitors (IC50 human MAO-B 0.612 nM, >16000-fold

261 Phe in this position (the sequence of sheep MAO B is unknown).

262 are without effect on either bovine or sheep MAO B or human MAO A.

263 asuring less than 12 A displayed significant MAO-B substrate properties.

264 ated by the addition of deprenyl, a specific MAO-B inhibitor.

265 synthetic glucocorticoid hormone, stimulates MAO B (an isoform of MAOs) promoter and catalytic activi

266 bottom halves of the lipid tails surrounding MAO-B are more and less ordered, respectively, than in t

267 faster (tau(1/2) = approximately 3 min) than MAO B (tau(1/2) = approximately 8 h).

268 These results indicate that MAO B expression is selectively induced by the activatio

269 Here we show that MAO B, but not MAO A, gene expression was induced during

270 These results suggested that MAO B gene expression is selectively induced by a decrea

271 sponse elements (RAREs) as identified in the MAO B 2-kb promoter, and mutation of the third RARE redu

272 ugh two clusters of Sp1-binding sites in the MAO B promoter.

273 Mutation of the CACCC element increased the MAO B promoter activity, and cotransfection with TIEG2 f

274 amily is important for the regulation of the MAO B gene expression.

275 l remained unchanged following a dose of the MAO B inhibitor pargyline at 2mg/kg.

276 Co-transfection of the MAO B promoter with dominant negative forms of Ras, Raf-

277 inhibit the PMA-dependent activation of the MAO B promoter.

278 Our data suggest that the MAO B oligomeric complexes are hexamers which contain th

279 , we propose that the coupling of FAD to the MAO B apoenzyme is a multistep process.

280 show that Egr-1 and c-Jun transactivate the MAO B promoter and increase endogenous MAO B transcripts

281 mission tomography and serial scans with the MAO B-specific radiotracers,l-[11C]deprenyl and deuteriu

282 maximum size that can be accommodated by the MAO-B active site.

283 ssed in terms of possible mechanisms for the MAO-B catalyzed oxidation of 1,4-disubstituted 1,2,3,6-t

284 trans analogues selectively target only the MAO-B isoform.

285 ctronic, polar, and steric parameters to the MAO-B-catalyzed oxidation of this type of cyclic tertiar

286 rahydropyridine (MPTP) is dependent upon the MAO-B (monoamine oxidase type B)-catalyzed production of

287 s a determinant for the specificity of these MAO B inhibitors and provides a molecular basis for the

288 Consistent with these, MAO-B protein level was much lower, whereas the amount o

289 Thus, MAO-B represents an attractive target for the treatment

290 ak3 (which are kinetic terms proportional to MAO B) were compared to identify organs that showed redu

291 erified to target brain MAO-A in addition to MAO-B.

292 B revealed lower [(3)H]lazabemide binding to MAO-B in the lateral and basal nuclei of the amygdala an

293 A modest elevation in binding to MAO-B observed in all amygdaloid nuclei in major depress

294 A significant decrease in binding to MAO-B was observed when cigarette smokers were compared

295 The specific binding of [(3)H]lazabemide to MAO-B was measured in the right amygdaloid complex of 15

296 2/CDCA7L/JPO2), that down-regulate MAO B via MAO B core promoter, which contains Sp1 sites.

297 y reinforces the need to investigate whether MAO-B inhibition may account for some of the behavioral

298 alogues were tested with MAO A and nine with MAO B.

299 ere used as adjuvant treatment compared with MAO-B inhibitors or dopamine agonists among people with

300 ylphenyl) analog 22 shows activity only with MAO-B.